VASOACTIVITY OF PROSTANOIDS IN THE TROUT (ONCORHYNCHUS-MYKISS) CORONARY SYSTEM - MODIFICATION BY NORADRENALINE

An isolated non-working trout heart, cannulated through the coronary a rtery and perfused with oxygenated saline with a coronary pressure hea d of 3.0 kPa has been used in this study. Effects on the coronary resi stance of catecholamines, thromboxanes (TXs) and prostacyclin (PGI2) w ere analyzed. The effects of PGI2 and TXs in presence of noradrenaline were also evaluated. Both adrenaline and noradrenaline vasoconstrict the trout coronary system, noradrenaline being more potent than adrena line. TXA2 induces 45% vasoconstriction at 10(-6)M, while TXB2 at the same concentration is a slight vasodilator. PGI2 acts as a weak vasodi lator (about 20% decrease in resistance at 10(-6)M). In presence of 10 (-7)M noradrenaline, 10(-8)M TXA2 reduces the vasoconstriction induced by the catecholamine alone from 60% to about 15%. Under similar condi tions, 10(-9)M PGI2 potentiates the vasoconstrictive response induced by noradrenaline while a much higher PGI2 concentration (10(-6)M) comp letely abolishes the vasoconstriction. The beta-receptor antagonist pr opranolol induces vasoconstriction, and 10(-9)M PGI2 in presence of pr opranolol further increases the vasoconstriction. The alpha-receptor a ntagonist phentolamine induces vasodilation and 10(-9)M PGI2 does not affect coronary resistance induced by phentolamine. These results impl y a possible interaction between noradrenaline and prostanoids (TXs an d PGI2) in the vasomotion of trout coronary system.